Abstract 20606: Persistent Low Oxygen Saturation During Sleep Predicts Impaired Pulmonary Vascular Response to Exercise in Patients With Sleep Disordered Breathing
Introduction: Sleep disordered breathing (SDB) is common among patients with cardiovascular disease, but its impact on physiologic responses to exercise remains unclear.
Hypothesis: We sought to determine the functional significance of SDB and low nocturnal oxygen saturation (SaO2) on hemodynamic responses to exercise.
Methods: We investigated subjects who underwent invasive cardiopulmonary exercise tests (iCPET) to evaluate dyspnea of unclear etiology who had evidence of SDB defined as an apnea hypopnea index (AHI) > 5 events/hour during a formal sleep study done within 3 years of the iCPET. Mean pulmonary artery pressure (mPAP) and mean wedge pressure (mPW) were indexed to cardiac output (CO) during exercise, with a mPAP-CO slope > 3 mmHg·min·L(-1) and a mPW-CO slope > 2 mmHg·min·L(-1) indicating an abnormal pulmonary vascular (PV) response to exercise.
Results: A total of 120 patients (mean±SD age 58.2 ± 12.6 years, body mass index 31.6 ± 7.5) with SDB (mean AHI 18.9 ± 21.3) and reduced SaO2 during the sleep study (minimal SaO2: 83± 7%, percentage of sleep-time with SaO2 < 90%: 8 ± 16%) were included in the analysis. Peak VO2, % predicted peak VO2, mPAP-CO and mPW-CO slope of the subjects were 15.9 ± 4.8 mL/min/kg, 75.9 ± 18.1%, 2.8 (IQR 1.52), and 2.2 ± 1.2 respectively, showing moderate to severely decreased exercise capacity and a mild degree of post-capillary exercise pulmonary hypertension. While AHI was not consistently related to hemodynamic responses to exercise, a lower minimal SaO2 inversely correlated not only with peak VO2 (r= -0.22, p = 0.03), but also with mPAP and mPW at peak exercise (r = -0.22, p = 0.03 and r= -0.2, p = 0.05). Also, the percentage of sleep time with SaO2 < 90 % positively correlated with mPAP at rest (r = 0.31, p = 0.01) and mPAP during exercise (r = 0.22, p =. 0.03). After adjusting for body mass index and the presence of known heart failure with preserved ejection fraction, these associations remained significant.
Conclusions: The magnitude and duration of reduced SaO2 during sleep is related to degree of impairment in exercise capacity and pulmonary hemodynamic responses to exercise among patients with dyspnea on exertion. Persistent low nocturnal SaO2 correlates better than AHI with impaired PV response to exercise.
- Sleep apnea
- Pulmonary function
- Cardiopulmonary exercise testing
- Exercise tests and training
- Heart failure, adult
Author Disclosures: E. D’Elia: None. R. Malhotra: None. C.S. Bailey: None. L. Wooster: None. P. Ferrero: None. C. White: None. K. Bakken: None. S. Perlini: None. M. Senni: None. G.D. Lewis: Other Research Support; Significant; Abbott Vascular, Novartis, Stealth, Shape Systems. Consultant/Advisory Board; Significant; Sonivie.
- © 2016 by American Heart Association, Inc.